Prevalence of feline infectious peritonitis in specific cat breeds

Original article: Prevalence of feline infectious peritonitis in specific cat breeds; 1.2.2006; Translation 28.2.2021

Loretta D. Pesteanu-Somogyi, DVM †, Christina Radzai, DVM Bar, Barrak M. Pressler, DVM, DACVIM


Although purebred cats are known to be more likely to develop feline infectious peritonitis (FIP), previous studies have not examined the prevalence of the disease in individual breeds. During 16 years, all cats diagnosed with FIP were identified at the University Veterinary Hospital. The breed, sex and reproductive status of the affected cats were compared with the general cat population and with mixed cat breeds evaluated during the same period. As in previous studies, sexually intact cats and purebred cats were significantly more likely to be diagnosed with FIP; the prevalence of the disease was also higher in males and young cats. Abesian, Bengal, Burmese, Himalayan, Ragdoll and Rex cats showed a significantly higher risk, while Burmese, Exotic Shorthair, Manx, Persian, Russian Blue and Siamese cats did not show an increased risk of developing FIP. Although other factors undoubtedly affect the relative prevalence of FIP, this study provides further guidance in prioritizing differential diagnoses in sick purebred cats.

Feline infectious peritonitis (FIP) is a progressive systemic disease with a wide range of clinical symptoms and high mortality (Hartmann 2005). It is caused by a mutation in feline enteric coronavirus, a common feline pathogen that may not cause any clinical signs or only transient diarrhea (Pedersen 1995; McReynolds and Macy 1997; Hartmann 2005). The mutated FIP virus spreads through the monocyte phagocytic system, and variations in the immune response of individual cats cause one of two recognized forms of the disease (Pedersen 1995, McReynolds and Macy 1997, Hartmann 2005). The "wet" form of FIP, which is observed in approximately 75% cases, is caused by complement-mediated vasculitis initiated by deposition of the immune complex in the vessel walls and usually leads to effusions in the body cavity (Pedersen 1995; McReynolds and Macy 1997, Hartmann 2005.). The "dry" form of FIP, identified in other cases, arises when a cell-mediated immune response dominates and granulomas form in various organs (Pedersen 1995; McReynolds and Macy 1997; Hartmann 2005).

Epidemiological studies of cats with FIP have identified several risk factors for developing the disease. The highest prevalence is in young cats (aged 3 months to 3 years), with most cases (75%) being in an environment with numerous cats (Kass and Dent 1995, Pedersen 1995, Foley et al. 1997a, McReynolds and Macy 1997, Rohrbach et al., 2001). Males and sexually intact cats are also at increased risk of developing FIP (Robison et al. 1971; Rohrbach et al. 2001). Other factors that are mentioned less frequently, associated with an increased prevalence of the disease, include seasonal (more cases are usually diagnosed in winter) FeLV infection, increased factors associated with "stress", high titers of coronavirus antibodies, regular feeding of new cats. to kennels and increased coronavirus excretion (Kass and Dent 1995, Pedersen 1995, McReynolds and Macy 1997, Foley et al. 1997a, Rohrbach et al. 2001).

Two studies report that FIP is more common in purebred cats (Robison et al. 1971; Rohrbach et al. 2001). Although the relative prevalence of FIP in different breeds of cats has been the subject of at least one study, statistical differences have not been calculated (Scott 1991). Therefore, to the authors' knowledge, it has never been thoroughly examined whether there is a specific predisposition to FIP depending on the breed. The purpose of this study was to determine whether such a preference for the cat breed actually exists. The sex and age of the affected cats were also examined to allow some comparison between the current population in the study and the populations from previous studies.

Materials and methods

The final diagnosis was checked for all cats entered into the computer database of patients at North Carolina State University College of Veterinary Medicine (NCSU-CVM) between December 22, 1986 and December 22, 2002. Cats with FIP were identified using coding terms. "Feline infectious peritonitis" or "FIP". In all cases, the final diagnosis was made by the attending physician; diagnostic criteria and the results of anti-mortem or post-mortem diagnostic test results have not been reviewed.

The breed, sex, and reproductive status of all cats examined at NCSU-CVM during the 16-year study period were assessed; all cats of unknown breed were excluded. Mixed breeds of cats of all coat lengths (domestic short-haired, medium and long-haired) were considered as a single breed (called "mixed breed") for data analysis purposes. Descriptive statistics were calculated for each variable studied for the FIP population and for the total cat population. Descriptive statistics on the age of cats at the time of evaluation were calculated only for cats affected by the FIP. Differences in breed, sex, and reproductive status were compared using Fisher's exact test; P values less than or equal to 0.05 were considered significant. The odds ratio (OR) and 95% confidence interval (CI) were also calculated for each variable.

The results

During the 16-year study period, 11,535 cats of known breeds were examined at the NCSU-CVM. The cats studied included mixed breeds of cats (9511 cats) and 36 different purebred breeds (2024 cats). Sixty cats (0.52%) had a definitive diagnosis of FIP; the breed was intended for all affected cats. Gender and reproductive status information was available for 57 of the 60 FIP cats and 11303 of the 11475 FIP negative cats. Age information was available for 58 of the 60 FIP cats.

Cats diagnosed with FIP included mixed breeds of cats (33 cats) and 13 different purebred breeds (27 cats). The prevalence of FIP in the mixed cat breed population was 0.35% versus 1.3% in the purebred cat population (Fig. 1). Purebred cats showed a significantly higher probability of developing FIP than mixed breeds (OR 4.5, CI 2.7-7.5; P <0.001). Breeds with a FIP prevalence significantly higher than that of mixed cat breeds included the Abyssinian, Bengal, Birman, Himalayan, Ragdoll and Rex breeds (including Cornish and Devon varieties) (Table 1, Figure 2). The prevalence of FIP in Burmese, exotic shorthair, Manx, Persian, Russian blue and Siamese cats did not differ significantly from mixed breed cats. Although two Havana cats evaluated at NCSU-VTH during the study period were diagnosed as FIP positive, this small number precluded statistical analysis.

Figure 1: Prevalence of FIP by group of cats
Figure 2: Prevalence of feline infectious peritonitis (FIP) in mixed breeds of cats and in breeds with a prevalence of FIP significantly different (P <0.05) from mixed breeds of cats.
TribeandCats diagnosed with FIP / total number of cats (% affected by FIP)Odds ratioConfidence intervalP value (Fisher's exact test)
Abesín cat3/99 (3.0%)8.982.71-29.770.006
Bengal cat1/8 (12.5%)41.034.91-342.850.028
Burma4/18 (22.2%)82.0626.66-262.44<0.001
Burmese cat1/37 (2.7%)7.981.06-59.910.124
Exotic shorthair cat1/62 (1.6%)4.710.63-34.980.199
Havana cat2/2 (100%)_b_b_b
Himalayan cat4/364 (1.1%)3.191.12-9.060.046
Manx1/67 (1.5%)4.350.59-32.290.213
Persian cat4/481 (0.5%)2.410.85-6.830.101
2/13 (15.3%)52.2211.14-244.790.001
Rex (Cornish and Devon)2/17 (11.7%)38.298.42-174.150.002
Russian blue1/39 (2.6%)7.561.01-56.680.130
Siamese cat1/536 (0.2%)0.540.07-3.931.00
Table 1: Prevalence, odds ratios and confidence intervals in purebred cats with FIP
and Breeds with 0.0% prevalence of feline infectious peritonitis are not listed.
b Insufficient number of cats for statistical calculations.

The prevalence of FIP was zero in 23 cat breeds. These included Angora (11 cats evaluated during the study period), Balinese (25 cats), Belgian (two cats), Bombay (four cats), British Blue (two cats), British Shorthair (three cats), Carthusian (four cats) , Colorpoint Shorthair (one cat), Egyptian Mau (one cat), Japanese bobtail (six cats), Korat (five cats), Maine Coon (151 cats), Maltese (two cats), Norwegian Forest (five cats), Ocicat ( 16 cats), Ragamuffin (one cat), Scottish Fold (15 cats), Siberian (one cat), Snowshoe (two cats), Somali (three cats), Sphinx (one cat), Tonkin (18 cats) and Turkish Van ( two cats). Unfortunately, the low prevalence of FIP in the population of mixed cat breeds has prevented the determination of significance or relative risk in these purebred cat varieties.

FIP was significantly more likely in sexually intact cats compared to the general cat population, regardless of gender (intact male versus neutered male, P <0.001; intact female versus neutered female, P = 0.002; all intact cats versus all neutered cats, P < 0.001, the prevalence of intact cats in the general population was 15.8%, compared to 45.6% in the FIP population). Although FIP was more numerous in males than in females, the difference in prevalence was not statistically significant (P = 0.425; 53.6% from the total cat population were males, compared to 59.6% from the FIP population). At the time of the last evaluation, the median age of cats with FIP was 0.96 years (25th percentile 0.5 years, 75th percentile 2.0 years). 67% cats with FIP were less than 2 years old.


Although an increased prevalence of FIP in purebred cats has been reported previously, this is the first time that the predisposition of specific breeds to disease development has been investigated (Robison et al. 1971; Rohrbach et al. 2001). Our results show that some breeds may in fact be more likely to develop FIP, especially Biri, Ragdoll, Bengal, Rex, Abesian and Himalayan breeds. Other cat breeds, Burmese, Exotic Shorthair, Manx, Persian, Russian Blue and Siamese, do not appear to be at increased risk compared to mixed cats. Our results regarding the effect of gender, reproductive status, and age on the relative prevalence of FIP are similar, although not identical, to previous studies (Robison et al. 1971, Horzinek and Osterhaus 1979; Kass and Dent 1995; Rohrbach et al. 2001).

Previous evidence supports the influence of host genetics on feline enteric coronavirus mutation or FIP susceptibility. Cheetahs whose genome has become more homozygous with minimal allelic diversity due to evolutionary narrowing have a very high prevalence of FIP (O '; Brien et al 1985). Likewise, the increased prevalence that we found in some variations of purebred breeds could be due to the concentration of inherited factors through breeding or small founding populations. Given the common environment and the virus strain, Foley and Pedersen (1995) calculated that slightly more than 50% susceptibility to FIP in purebred cats from six farms can be attributed to inherited differences between individuals. Interestingly, in this study, one of the kennels with numerous closely related cats suffering from FIP was the Biriem kennel (Foley and Pedersen 1995). In this study, Burmese were by far the most affected, so we may not be the first to point out the increased sensitivity to FIP in this breed.

Other researchers have questioned whether the increased prevalence of FIP in purebred cats could not actually be due to misleading factors. Purebred cats are bred more frequently in kennels, which can be inherently more stressful due to the environment with numerous cats, the regular arrival of new cats and frequent breeding (Kass and Dent 1995, Pedersen 1995). In addition, kennel cats are likely to face higher exposure to feline enteric coronavirus (a condition for FIP development) due to increased population density (Foley et al. 1997a, 1997b, McReynolds and Macy 1997). Finally, the possible increased willingness of owners of expensive purebred cats to perform advanced diagnosis and supportive care at a recommended veterinary facility, such as NCSU-VTH, may skew the apparent prevalence of the disease. However, these factors are expected to falsely increase the prevalence of FIP in all purebred cats, and not only in those breeds that we report have an increased risk of developing the disease.

We have decided to include in this report cases based on the final diagnosis entered in our computerized medical database, and not on the control of records and histopathological reports. As a result, we must recognize that future investigations, which will be limited to cases with a confirmed diagnosis, may yield different results. However, because the pre-death diagnosis of FIP in our tertiary care hospital is expected to be similar to the diagnostic algorithms proposed by other authors, we feel that our results, especially in breeds with more or a particularly strong association with the disease, are unlikely to conflict with future studies. (Sparkes et al. 1991, Rohrer et al. 1993, Addie and Jarrett 1998).

A multivariate analysis of the variables studied here would further define the susceptibility of a specific breed to FIP. For example, it is not known whether breeds with an increased FIP prevalence actually had a higher number of intact cats, which affected our calculations. Furthermore, very few individuals were examined in some breeds and the large CI reflected inaccuracy in risk determination. We doubt that the absence of cats diagnosed with FIP in 23 breeds indicates absolute disease resistance, although it is possible that some of these breeds (such as the Maine Coon cat, which were observed in relatively large numbers at NCSU-VTH) have unrecognized protective factors. which affect susceptibility to FIP. Unfortunately, due to the low prevalence of FIP in all cats, a much larger population will need to be examined to determine if the low incidence of the disease in these breeds is statistically significant.

The predisposition of certain breeds to the development of FIP demonstrated here requires further research. Our results suggest that in some sick purebred cats, the suspected FIP index is likely to increase. A multicenter study, which includes cases from both primary and recommended facilities with multivariate analysis, is probably necessary to definitively answer the question of the sensitivity of individual breeds to FIP.


We thank Cavell Brownie, PhD (Department of Statistics, State University of North Carolina) for performing statistical analyzes, and Malcolm Roberts, BVSc, PhD, MPH, FRCVS, FACVSc (Department of Clinical Sciences, State University of North Carolina) for reviewing the manuscript.


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